Telomeres are the protective ends of our chromosomes that naturally shorten with age. Although the cells were only grown in a petri dish and not implanted back into a person, the study marks a major step forward in controlling, and even reversing, the cellular aging process.

Researchers from Houston Methodist Research Institute (HMRI) used a new technique to introduce RNA into the DNA of cells taken from patients with progeria, a genetic disease that causes individuals to age at an accelerated rate. As a result, the RNA introduction caused the cells to create more telomerase, a key component in telomeres. In turn, this caused the telomeres to grow longer, Motherboard reported.

The age-reversed cells were not implanted back into people, which means that we aren’t sure if the age-reversal can last or what implications it may have. In addition, while telomeres are associated with aging, the correlation is not exactly perfect, as some older individuals can have longer telomeres than younger people. So, it could be that telomere extension may work in theory, but in reality, has little or no effect on our health. Lengthening telomeres could also have some serious consequences, such as increasing cancer risk, Dr. Peter Lansdorp, a professor of medical genetics at the University of British Columbia and scientist at the BC Cancer Agency, told Motherboard.

Lengthening telomeres may hold the key for finally creating an effective treatment for children with protergia. In addition, telomere lengthening may not only add more time to your cells’ life spans, it could also reverse some of the damage caused by aging.------------------

What effect on aging do you think this would have if it actually works in living humans? Would undo certain parts of aging, or make it easier to deal with? Would it drastically extend life expectancy or just be a niche treatment for a few specific diseases?

Or why does the public generally agree with doctors' H.oath and with govt's protection of the pursuit of happiness, but disagree (electorally) with living healthier and longer IOW more of the same thing they already approve of?

You can do anything you want with laws except make Americans obey them. | What I want to do is to look up S. . . . I call him the Schadenfreudean Man.

Telomeres are the protective ends of our chromosomes that naturally shorten with age. Although the cells were only grown in a petri dish and not implanted back into a person, the study marks a major step forward in controlling, and even reversing, the cellular aging process.

Researchers from Houston Methodist Research Institute (HMRI) used a new technique to introduce RNA into the DNA of cells taken from patients with progeria, a genetic disease that causes individuals to age at an accelerated rate. As a result, the RNA introduction caused the cells to create more telomerase, a key component in telomeres. In turn, this caused the telomeres to grow longer, Motherboard reported.

The age-reversed cells were not implanted back into people, which means that we aren’t sure if the age-reversal can last or what implications it may have. In addition, while telomeres are associated with aging, the correlation is not exactly perfect, as some older individuals can have longer telomeres than younger people. So, it could be that telomere extension may work in theory, but in reality, has little or no effect on our health. Lengthening telomeres could also have some serious consequences, such as increasing cancer risk, Dr. Peter Lansdorp, a professor of medical genetics at the University of British Columbia and scientist at the BC Cancer Agency, told Motherboard.

Lengthening telomeres may hold the key for finally creating an effective treatment for children with protergia. In addition, telomere lengthening may not only add more time to your cells’ life spans, it could also reverse some of the damage caused by aging.------------------

What effect on aging do you think this would have if it actually works in living humans? Would undo certain parts of aging, or make it easier to deal with? Would it drastically extend life expectancy or just be a niche treatment for a few specific diseases?

As a cynic, I expect it to increase the chances of Cancer, but it will be wonderful if it does not.

And I loved the David Eddings books.

‘What all the wise men promised has not happened, and what all the damned fools said would happen has come to pass.’ — Lord Melbourne —

An RNA vaccine or treatment could be developed to do this. It could even be done in a home lab and be even cheaper to develop than the CRISPR therapy Liz Parrish developed in her home lab to accomplish the same purpose two years ago.

However, I think it unlikely that telomere shortening is a major cause of aging. I think its an effect rather than cause. I still maintain the primary cause of aging is mitochondrial dysfunction (either mDNA damage or damage to the mPTP), a therapy to fix which can also be developed in the near future.

Accumulation of senescent cells appears to also be a major cause of aging. There are already start-up companies (is there ANYTHING that cannot be accomplished through entrepreneurship?) develop treatments for this as well.

kurt9 wrote: I still maintain the primary cause of aging is mitochondrial dysfunction (either mDNA damage or damage to the mPTP), a therapy to fix which can also be developed in the near future.

From what i've read, mitochondrial dysfunction appears to be the primary reason why cells go into senescence. Once their own powerplant fails, cells have to drain material off of their neighbors. Not only does this turn them parasitical, they start releasing toxins that also damage other cells.

Quercitin supposedly helps remove senescent cells. There has been a few reports about it in the last year. Not a cure, but perhaps a prolonging action.

‘What all the wise men promised has not happened, and what all the damned fools said would happen has come to pass.’ — Lord Melbourne —

kurt9 wrote: I still maintain the primary cause of aging is mitochondrial dysfunction (either mDNA damage or damage to the mPTP), a therapy to fix which can also be developed in the near future.

From what i've read, mitochondrial dysfunction appears to be the primary reason why cells go into senescence. Once their own powerplant fails, cells have to drain material off of their neighbors. Not only does this turn them parasitical, they start releasing toxins that also damage other cells.

Quercitin supposedly helps remove senescent cells. There has been a few reports about it in the last year. Not a cure, but perhaps a prolonging action.

One of the things that convinced me that mitochondrial dysfunction is the root cause of aging was Nick Lane's book "Power, Sex, and Suicide: Mitochondria and the Meaning of Life". I read this book about 10 years ago. It convinced me of two things. One, mitochondrial dysfunction is the primary cause of aging and, two, that we are likely alone in this galaxy at least, if not the observable universe.

kurt9 wrote:One of the things that convinced me that mitochondrial dysfunction is the root cause of aging was Nick Lane's book "Power, Sex, and Suicide: Mitochondria and the Meaning of Life". I read this book about 10 years ago. It convinced me of two things. One, mitochondrial dysfunction is the primary cause of aging and, two, that we are likely alone in this galaxy at least, if not the observable universe.

I haven't read that book, but I am mostly of the same opinion that you have.

‘What all the wise men promised has not happened, and what all the damned fools said would happen has come to pass.’ — Lord Melbourne —

hanelyp wrote:Indeed, shortening telomeres are but one of several elements of cellular aging. Unless other factors are also accounted for increased cancer seems a risk.

Endocannabinoids naturally scavenge cancerous cells. It is too bad that research on that in America is stymied by our laws. Maybe Congress will fix that. Something like 70% to 90% of voting age Americans think that should be done.

No matter. Israel has a strong research program in place.

Engineering is the art of making what you want from what you can get at a profit.

kurt9 wrote: I still maintain the primary cause of aging is mitochondrial dysfunction

From what i've read, mitochondrial dysfunction appears to be the primary reason why cells go into senescence. Once their own powerplant fails, cells have to drain material off of their neighbors.

Quercitin supposedly helps remove senescent cells.

Quercitin has only been shown to be highly effective in mice when combined with a very toxic dasatinib(chemo drug). Its solo impact has been modest. The study that showed a 25% increase in life expectancy was a Quercitin and Dasatinib combo(they appear to have a synergistic effect).

kurt9 wrote: I still maintain the primary cause of aging is mitochondrial dysfunction

From what i've read, mitochondrial dysfunction appears to be the primary reason why cells go into senescence. Once their own powerplant fails, cells have to drain material off of their neighbors.

Quercitin supposedly helps remove senescent cells.

Quercitin has only been shown to be highly effective in mice when combined with a very toxic dasatinib(chemo drug). Its solo impact has been modest. The study that showed a 25% increase in life expectancy was a Quercitin and Dasatinib combo(they appear to have a synergistic effect).

Belgarath wrote:Quercitin has only been shown to be highly effective in mice when combined with a very toxic dasatinib(chemo drug). Its solo impact has been modest. The study that showed a 25% increase in life expectancy was a Quercitin and Dasatinib combo(they appear to have a synergistic effect).

I have been on Quercetin for years now before I even knew it was a "senolytic"; not brave enough to try the Dasatinib; although I understand you only need to take the two together once every few years to clear out senescent cells

Belgarath wrote: So far the best senolytic found has been Fisetin.

Thanks...I had never heard of it; I understand though while there is no evidence of chronic use being harmful (to humans) there is not good long term study data on such either.